Hypothalamic CART is a new anorectic peptide regulated by leptin

Peter Kristensen (), Martin E. Judge, Lars Thim, Ulla Ribel, Kennet N. Christjansen, Birgitte S. Wulff, Jes T. Clausen, Per B. Jensen, Ole D. Madsen, Niels Vrang, Philip J. Larsen and Sven Hastrup
Additional contact information
Peter Kristensen: Health Care Discovery, Novo Nordisk A/S
Martin E. Judge: Health Care Discovery, Novo Nordisk A/S
Lars Thim: Health Care Discovery, Novo Nordisk A/S
Ulla Ribel: Health Care Discovery, Novo Nordisk A/S
Kennet N. Christjansen: Health Care Discovery, Novo Nordisk A/S
Birgitte S. Wulff: Health Care Discovery, Novo Nordisk A/S
Jes T. Clausen: Health Care Discovery, Novo Nordisk A/S
Per B. Jensen: Hagedorn Research Institute
Ole D. Madsen: Hagedorn Research Institute
Niels Vrang: University of Copenhagen
Philip J. Larsen: University of Copenhagen
Sven Hastrup: Health Care Discovery, Novo Nordisk A/S

Nature, 1998, vol. 393, issue 6680, 72-76

Abstract: Abstract The mammalian hypothalamus strongly influences ingestive behaviour through several different signalling molecules and receptor systems1,2,3,4. Here we show that CART (cocaine- and amphetamine-regulated transcript), a brain-located peptide5,6,7,8, is a satiety factor and is closely associated with the actions of two important regulators of food intake, leptin and neuropeptide Y. Food-deprived animals show a pronounced decrease in expression of CART messenger RNA in the arcuate nucleus. In animal models of obesity with disrupted leptin signalling, CART mRNA is almost absent from the arcuate nucleus. Peripheral administration of leptin to obese mice stimulates CART mRNA expression. When injected intracerebroventricularly into rats, recombinant CART peptide inhibits both normal and starvation-induced feeding, and completely blocks the feeding response induced by neuropeptide Y. An antiserum against CART increases feeding in normal rats, indicating that CART may be an endogenous inhibitor of food intake in normal animals.

Date: 1998
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DOI: 10.1038/29993

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